Flashcards in AH1 Exam 3 Urinary/Renal Deck (229):
clinically significant UTI, symptoms arise at 10^2-10^3
typically identified as the causative microorganism for UTI associated with broad spectrum antimicrobial antibiotic therapy or indwelling catheter
fever, chills, and flank pain
indicated UTI in upper urinary tract (involving renal parenchyma, pelvis, and ureters)-pyelonephritis
inflammation of renal parenchyma and collecting system
inflammation of the bladder wall
inflammation of the urethra
A UTI that has spread into the systemic circulation and is a life threatening condition requiring emergency treatment
infections that occur in an otherwise normal urinary tract and usually only involve the bladder
infections with coexisting presence of obstruction, stones, or catheters, existing diabetes or neurologic disease, pregnancy induced changes, of a recurrent infection
complications associated with a complicated UTI
pyelonephritis, urosepsis, and renal damage
term for a UTI due to original infection not being eradicated
unresolved bacteriuria or bacterial persistance
Lower ________ levels cause vaginal atrophy, a decrease in vaginal lactobacilli, and an increase in vaginal pH
**Giving women low dose intravaginal estrogen replacement acidifies the vagina and may be effective in treating recurrent UTI**
dysuria, frequent urination (+than q2h), urgency, and suprapubic discomfort or pressure
Urine may have blood or sediment
LUT (lower Urinary Tract) infection
nonspecific symptoms of UTI
characteristic symptoms of UTI are often absent in which population?
older adults who instead experience non localized abdominal discomfort, cognitive impairment, or generalized clinical deterioration
diagnostic study that identifies presence of nitrates, WBCs, and leukocyte esterase in urine
an enzyme present in WBCs that indicates pyuria
a voided midstream technique yielding a clean catch urine sample is preferred for obtaining which diagnostic test?
what do you do with urine after collecting it?
refrigerate it immediately!! and it should be cultured w/in 24 hrs of collection
two tests used when obstruction of the urinary system is suspected of causing UTI
intravenous pyelogram (IVP)
Renal ultrasound is preferred urinary tract imaging technique if recurrent UTI, bc it is noninvasive, easy to perform, and relatively inexpensive
Uncomplicated UTI antibiotics
Bactrim, Septra (trimethoprim-sulfamethoxazole)
Nacrodantin, Macrobid (nitrofurantoin)
short-term 1-3 days
Antibiotics 7-14 days or longer
Bactrim or Macrobid
Ampicillin, amoxicillin, first gen cephalosporin, fluoroquinolone
consider 3-6 mons trial of suppressive or prophylactic antibiotic regimen
consider post coital antibiotic prophylaxis (Bactrim, Macrobid, or Cephalexin)
adequate fluid intake
Complicated UTI treatment
Nitrofurantoin (Macrodantin, Macrobid) patient teaching
avoid sunlight, notify HCP if fever, chills, cough, chest pain, dyspnea, rash or numbness or tingling of fingers or toes develops
debilitated persons, older adults, patients who are immune compromised due to co-morbid disease (CA, HIV, DM), and patients treated with immunosuppressive agents or corticosteriods
Are at increased risk of UTI
hyper/hypothermia, decreasing BP, rapid pulse and RR, warm flushed skin
report to HCP as these may indicate septic shock r/t urosepsis
benefits of increased fluid intake during UTI, pyelonephritis
fluids will increase frequency of urination at first, but will also dilute the urine, making the bladder less irritable. Fluids will help flush out bacteria before they colonize in the bladder.
Caffeine, alcohol, citrus juices, chocolate, and highly spiced foods or bevs
should be avoided during UTI as they are irritating to the bladder
nonpharmacological relief of UTI
heating pad, warm shower, sitz bath
commonly starts in renal medulla and spreads to renal cortex
mild fatigue, sudden onset of chills, fever, vomiting, malaise, flank pain, and the LUTs of cystitis (dysuria, urgency, frequency).
Costovertebral tenderness is usually present on the affected side
these manifestations usually subside within a few days (even without treatment) but bacteriuria and pyuria persist
CBC shows leukocytosis and a shift to the left with an increase in immature neutrophils (bands)
kidneys have become small, atrophic, and shrunken and have lost fxn owing to scarring or fibrosis. Usually the outcome of recurrent infections of upper urinary tract
Chronic pyelonephrits (AKA interstitial nephritis, chronic atrophic pyelonephritis, or reflux nephropathy)
*if both kidneys are involved, often progresses to ESRD
how do you diagnose chronic pyelonephritis?
*radiologic imaging-indicate small, contracted kidney with thinned parenchyma; collecting system may be small or hydronephrotic
trichomona, monilial infection, chlamydial infection and gonorrhea
typical causes of urethritis
trimethoprim/sulfamethoxazole and nitrofurantoin
drugs for bacterial infections of urologic origin
Flagyl and Mycelex
nystantin (Mycostatin), Diflucan
teach patients with sexually transmitted urethritis to refer their sexual partner(s) for evaluation and testing if they have had sexual contact in the last ____ days
the result f obstruction and subsequent rupture of the periurethral glands into the urethral lumen with epithelization over the opening of the resulting periurethral cavity
urethral diverticula (mostly occurs near Skene's glands which are the largest and most distal glands along the urethra)
dysuria, post void dribbling, frequent urination, urgency, suprapubic discomfort or pressure, dyspareunia, and a feeling of incomplete bladder emptying; urinary incontinence is common; urine may contain gross hematuria and sediment (cloudy); an anterior vaginal wall mass may be noted on physical exam and the mass may be tender and expel purulent discharge through urethra when palpated.
urethral diverticula (1:4 women will have no symptoms)
Voiding Cystourethrography (VCUG)
UA, MRI to determine size of diverticulum
condition suspected whenever a pt experiences symptoms of a UTI but tests are neg for bacteria or pyuria
Interstitial Cystitis/Painful Bladder Syndrome:
avoid acidic foods: citrus, aged cheese, nuts, vinegar, curries, hot peppers +tea, coffee, alcohol, soda
take calcium phosphorus supplements
bladder irritating foods and dietary recommendations (esp for IC/PBS)
Elavil and Aventyl are used to decrease burning pain and urinary frequency
Pentosan (Elmiron) is only oral agent approved for tx of IC-enhances protective effects of glycosaminoglycan layer of the bladder
drugs do not provide immediate relief!!** for that, give opioid analgesics!
instill Dimethylsulfoxide (DMSO) directly into bladder to desinsitize pain receptors in the bladder wall.
Heparin and hyaluronic acid may also be instilled in bladder
Instillations are often administered with Lidocaine
Bacille Calmette-Guerin is an attenuated form of Mycobacterium bovis, and is another common tx.
medication mgmt IC/PBS
affects both kidneys equally and is the third leading cause of renal failure in US
SLE, systemic sclerosis (scleroderma), streptococcal infection
common causes of glomerulonephritis
accumulation of antigen, antibody, and complement in the glomeruli:
lumpy bumpy deposits in renal tissue
hematuria and urinary excretion of RBCs, WBCs, and casts. Proteinuria, and elevated BUN/Cr
clinical manifestations of glomerulonephritis
develops 5-21 days after infection of the tonsils, pharynx, or skin (streptococcal sore throat, impetigo) (group A beta hemolytic strep)
Acute Poststreptococcal glomerulonephritis-due to complement clogging glomerulus
generalized body edema, hypertension, oliguria, hematuria with a smoky or rust appearance (indicative of bleeding in upper urinary tract), and proteinuria. Fluid retention (due to decreased glomerular filtration); abdominal or flank pain possible
Acute Poststreptococcal glomerulonephritis-
an immune response to streptococcus is usually demonstrated by assessment of
ASO titers (antistreptolysin-O)
which will reflect a decrease in complement componenets of C3 and CH50
to confirm Acute Poststreptococcal glomerulonephritis-
erythrocyte casts are usually indicative of __________ if found in dipstick urinalysis
Acute Poststreptococcal glomerulonephritis-
rest (address proteinuria, hematuria), sodium and fluid restriction (to address edema), diuretics (to address edema), anti-HTN therapy, adjustment of dietary protein (if BUN is elevated-to decrease nitrogenous waste in urine)
tx for Acute Poststreptococcal glomerulonephritis-
a cytotoxic autoimmune disease characterized by the presence of circulating antibodies against glomerular and alveolar basement membrane
Good Pasture Syndrome-seen mostly in young male smokers
flulike symptoms with pulmonary symptoms of cough, milk SOB, hemoptysis, crackles, rhonchi, and pulmonary insufficiency. hematuria, weakness, pallor, anemia, and renal failure
clinical manifestations of Good Pasture's Syndrome
corticosteroids, immunosuppressive drugs (Cytoxan, Imuran), plasmapheresis, and dialysis
tx for good pasture syndrome, rapidly progressive glomerulonephritis
HTN, edema, proteinuria, hematuria, and RBC casts
rapidly progressive glomerulonephritis
proteinuria, hematuria, and slow development of uremia
Chronic glomerulonephritis: protein and phosphate restrictions may slow disease progression
when the glomerulus is excessively permeable to plasma protein, causing proteinuria that leads to low plasma albumin and tissue edema
peripheral edema, massive proteinuria, HTN, hyperlipidemia, hypoalbuminemia, decreased serum albumin, decreased total serum protein, and elevated serum cholesterol; hypocalcemia, blunted calcemic response to parathyroid hormone, hyperparathyroidism, and osteomalacia
What causes hyperlipidemia?
the diminished plasma oncotic pressure from the decreasaed serum proteins (nephrotic syndrome) stimulates hepatic lipoprotein synthesis-->hyperlipidemia
nephrotic proteinuria (nephrotic syndrome) leads to
loss of clotting factors resulting a hypercoagulable state
serious complication of nephrotic syndrome
hypercoagulability with thromboembolism
ACEI's, NSAIDS, low sodium, low protein
if severe, consider corticosteriods and cyclophosphamide
tx for nephrotic syndrome
Nursing interventions r/t edema
weight pt daily, monitor I&Os, measure abdominal girth or extremity size
risk for imbalanced nutrition: less than body requirements
nephrotic syndrome from excessive loss of protein in the urine. serve small, frequent meals in a pleasant setting
stones assoc with UTI (magnesium ammonium phosphate)
abnormalities that result in increased urine levels of calcium, oxaluric acid, uric acid, or citric acid
metabolic risk factors for the development of urinary tract calculi
large intake of dietary proteins that increases uric acid excretion
excessive amounts of tea or fruit juices that elevate urinary oxalate level
large intake of calcium and oxalate
dietary risk factors for the development of urinary tract calculi
abdominal or flank pain, hematuria, and renal colic
clinical manifestations of urinary stones
sardines, herring, mussels, liver, kidney, goose, venison, meat soups, sweetbreads
foods high in purine (avoid if uric acid stones)
milk, cheese, ice cream, yogurt, all beans except green beans, lentils, fish with fine bones (sardines, kippers, herring, salmon), dried fruits, nuts, ovaltine, chocolate, cocoa
food high in calcium (avoid if calcium stones)
drak roughage, spinach, rhubarb, asparagus, cabbage, tomatoes, beets, buts, celery, parsley, runner beans, chocolate, cocoa, instant coffee, ovaltine, worcestershire sauce, tea
food high in oxalate
all voided urine should be strained through gauze or urine strainer
pts with urinary stones
hypertension, hematuria, feeling of heaviness in the back, side or abdomen, chronic pain, bilateral, enlarged kidneys are palpable
polycystic kidney disease, a hereditary renal disease characterized by a cortex and medulla filled with large, thin walled cysts that enlarge and destroy surrounding tissue by compression.
which type of urinary incontinence is more common in men?
which types of urinary incontinence are more common in women?
stress and urge incontinence
urinary leakage and post void dribbling
normal PVR (post void residual)
repeat measurement if you get a finding over 100mL
Abnormal PVR in older client
>200mL obtaining on two separate occasions and will require HCP attention
urinary retention is caused by two different dysfunctions of the urinary system:
1) bladder outlet obstruction (enlarged prostate)
2) deficient detrusor (bladder) muscle contraction strength (caused by childbirth, DM, overdistention, chronic alcoholism, anticholinergics)
sudden increase in intrabdominal pressure causes involuntary passage of urine (coughing, laughing, sneezing, heavy lifting, exercising
tx: Kegels, weight loss if obese, cessation of smoking, topical estrogen
condition occurs randomly when involuntary urination is preceded by urinary urgency. Overactive bladder, nocturnal frequency and incontinence are common
Treat underlying cause
bladder retraining with urge suppression, decrease in dietary irritants, bowel regularity, and kegels
administer anticholinergics, CCBs, or Tofranil at bedtime
what causes urge incontinence?
uncontrolled contraction or overactivity of detrusor muscle (CNS d/os, CVA, alzheimers, brain tumor, parkinsons, interstitial cystitis)
condition occurs when the pressure of urine in overfull bladder overcomes sphincter control; bladder remains distended and is usually palpable
urinary catheterization to decompress bladder
implement Crede or Valsalva maneuver
alpha blockers Cardura, Flomax
bethanechol to enhance bladder contractions
what causes overflow incontinence?
bladder or urethral outlet obstruction or underactive detrusor muscle caused by myogenic or neurogenic causes (herniated disc, diabetic neuropathy)
may occur after anesthesia and surgery
neurogenic bladder (flaccid type)
condition occurs when no warning or stress precedes periodic involuntary urination.
Treat underlying cause
bladder decompression to prevent ureteral reflux and hydronephrosis
intermittent self cath
diazepam and baclofen to relax external sphincter
What causes Reflux incontinence?
spinal cord lesion above S2 interferes with CNS inhibition resulting in detrusor hyperreflexia and interferes with pathways coordinating detrusor contraction and sphincter relaxation
loss of urine resulting from cognitive, functional or environmental factors
modifications of environment or care plan that facilitate regular, easy access to toilet and promote patient safety
penile compression device
must be released hourly to void
drugs to decrease bladder spasms
oxybutynin or other oral antispasmodics or belladonna and opium
irrigating a nephrostomy tube
no more than 5mL sterile saline solution at one time to prevent overdistention of the kidney; infection and kidney stones are complications assoc with nephrostomy tubes
inserting a urethral catheter q3-5h; somtimes only twice a day to measure residual volume and to ensure empty bladder
how frequently do you change a catheter?
most common cause of acute kidney injury
acute tubular necrosis
most common cause of chronic kidney disease
diagnostic criteria for acute kidney disease
acute reduction in urine output and/or elevation in serum Cr
diagnostic criteria for CKD
GFR 3mos and/or kidney damamge > 3mos
Kidney failure results in an inability to excrete ______ and ____ as well as contributing to disturbances of all body systems
metabolic waste and water
an accumulation of nitrogenous waste products (urea nitrogen and creatinine) in the blood
AKI develops over hours or days with progressive elevations of ____, ______, and _____
BUN, Creatinine, and potassium
factors external to the kidneys that reduce systemic circulation causing a reduction in renal blood flow, and lead to decreased glomerular perfusion and filtration of the kidneys.
Prerenal causes of AKI
hypovolemia, decreased CO, Decreased PVR, decreased renovascular blood flow
Why might renovascular blood flow diminish?
bl renal vein thrombosis
renal artery thrombosis
Prerenal azotemia results in
a reduction in the excretion of sodium (less than 20 mEq/L) increased salt and water retention, and decreased urine output due to activation of angiotensin II, aldosterone, NE, and ADH
Prerenal conditions account for many cases of
intrarenal AKI bc if the decreased perfusion persists for an extended period of time, the kidneys lose their ability to compensate and damage to renal tissue occurs
What damages intrarenal function?
prolonged ischemia, nephrotoxins (aminoglycoside antibiotics, contrast medium), hemoglobin released from hemolyzed RBCs, or myoglobin released from necrotic muscle cells
Primary renal disease such a acute glomerulonephritis, acute tubular necrosis, or SLE may also cause AKI
Most common cause of intrarenal AKI
Acute tubular necrosis
what causes Acute tubular necrosis?
ischemia, nephrotoxins, or sepsis
what causes postrenal causes of AKI?
mechanical obstruction in the outflow of urine
spinal cord disease
trauma to back, pelvis, or perineum
Where does the urine goes if obstructed?
it refluxes into renal pelvis, impairing kidney fxn
hydronephrosis (due to BL ureter obstruction and urine builds up in renal pelvis)
phases of AKI
oliguria-high urine specific gravity, hyperkalemia, hypervolemia *give only enough fluids in oliguric phase to replace losses (400-500mL/24hrs)
diuretic (low urine specific gravity (<1.020g/mL), hypokalemia, hypovolemia
recovery: everything returns to normal
RIFLE standardizes the diagnosis of AKI
Risk (serum Cr increases X1.5 or GFR decreased by 25%
Injury CrX2 or GFR decreased by 50%
Failure CrX3 or GFR decreased by 75% or Cr>4mg/dL
Loss persistent Acute Kidney Failure; complete loss of kidney fxn if >4wks
End Stage Renal Disease complete loss of kidney fxn > 3 mos
less than 400mL/day or urine
oliguria; urine specific gravity will be high (>1.020g/mL)
typical duration of oliguria phase of AKI
10-14 days but can last for months in some cases
the longer the oliguric phase
the poorer the prognosis for complete recovery of kidney fxn
often seen in urinary obstruction (postrenal failure)
often seen in prerenal failure
seen with Acute interstitial nephritis and ATN
anuria and oliguria can lead to
JVD, edema, HTN, fluid overload, HF, pulmonary edema, pleural effusions
In kidney failure, the kidneys cannot synthesize
ammonia which is needed for hydrogen excretion leading to metabolic acidosis (bicarb is used up trying to neutralize the hydrogen ions that can't be excreted)--> Kussmaul respirations
(with regard to AKI) uncontrolled hyponatremia or water excess can lead to
(With regard to AKI) What happens to potassium in AKI?
kidneys cannot excrete potassium--> hyperkalemia
compounded by massive tissue trauma bc damaged cells release addt'l potassium into ECF.
PLUS bleeding and blood tranfusions may cause cellular destruction, releasing MORE potassium into ECF
FINALLY, Acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out of the cells into the ECF
peaked T waves, widening QRS complex, and ST depression
What happens to the blood with AKI?
leukocytosis-the most common cause of death with AKI is INFECTION (in urinary and respiratory systems)
AKI with leukopenia and thrombocytopenia indicate
etiology of SLE or thrombotic thrombocytopenic purpura
A CBC with esinophilia in a pt with AKI indicates
etiology of allergic response and presence of interstitial nephritis
an end product of endogenous muscle metabolism
end product of protein metabolism
BUN and Cr are __________ in AKI
what does an elevated BUN indicate?
dehydration, corticosteriods, catabolism r/t infections, fever, severe injury, or GI bleeding, thus elevated Cr is more indicative of AKI
fatigue, difficulty concentrating which escalates to seizures, stupor, and coma
neurologic changes that occur as nitrogenous wastes accumulate in brain and other nervous tissue
flapping tremor when the wrist is extended
What happens during the diuretic phase of AKI?
kidneys have regained ability to excrete waste, but not to concentrate urine in the tubules and thus hypotension and hypovolemia result from the massive fluid losses (3-5L/day!)
How long does diuretic phase of AKI last
What happens in the recovery phase of AKI?
GFR increases, allowing the BUN/Cr to plateau then decrease. Major improvements occur within 1-2 weeks of this phase, but kidney fxn may take up to 12 mos to stabilize
dehydration, blood loss, severe heart disease
prerenal causes of AKI
nephrotoxic drugs, recent blood transfusion, or radiologic study using contrast media
intrrenal causes of AKI
stones, BPH, CA of bladder or prostate
postrenal causes of AKI
Urine sediment (obtained in urinalysis) containing abundant casts, cells, or proteins (hematuria, pyuria, and crystals) suggest
urine sediment may be normal in
prerenal and postrenal AKI
assess abnormalities in kidney blood flow, tubular fxn, and the collecting ststem
identify lesions and masses , obstructions or vascular abnormalities in kidney
administration of contrast medium gadolinium (used primarily in MRA) has been associated with the development of
nephrogenic systemic fibrosis: cutaneous hyperpigmentation and induration and joint contractures
diagnosis of intrarenal cause of AKI
during the oliguric phase, monitor fluid intake closely. fluid restrictions often are
600mL plus previous 24 hr fluid loss
what temporarily shifts potassium back into cels during hyperkalemia?
insulin and sodium bicarb
what rises threshold at which hyperkalemia related dysrhythmias will occur?
what removes potassium from the body during aki and hyperkalemia?
kayexalate and dialysis
when is kayexalate contraindicated?
paralytic ileus bc bowel necrosis may occur
What is RRT?
renal replacement therapy
Continuous hemodialysis (CRRT over 24 hours-slowly)
When do you institute RRT?
1) volume overload causing compromised cardiac/respiratory fxn
2) elevated serum potassium
3) metabolic acidosis (bicarb 120mg/dL
5)significant change in mental status
6) pericarditis, pericardial effusion, or cardiac tamponade
what to consider when giving iv insulin for elevated k+?
give glucose iv concurrently to avoid hypoglycemia
how do you give kayexalate?
by mouth or retention enema; mixed in water with sorbitol to produce osmotic diarrhea, allowing for evacuation of potassium rich stool from the body
What might you hear in a heart with aKI
s3 gallop, murmurs, pericardial friction rub
dont give a patient with renal d/o a contrast medium diagnostic study. If you cant avoid it...
ensure optimal hydration using bicarbonate solution or sodium chloride with or without the prophylactic administration of mucomyst
1 kg =
1000 ml of fluid
what causes stomatitis?
ammonia excess in saliva irritates mucus membranes
stage 1 CKD
Stage 2 CKD
GFR 60-89 mL/min/1.73^2
Stage 3 CKD
GFR 30-59 Moderately decreased GFR
Stage 4 CKD: prep for RRT
GFR 15-29 severe decrease in GFR
Stage 5 CKD
GFR <15 or dialysis required KIDNEY FAILURE
two main causes of CKD
a syndrome in which kidney function declines to the point that symptoms develop in multiple body systems
Uremia in CKD
n/v, lethargy, fatigue, impaired thought processes and HA
CKD: Altered carb metabolism
due to impaired glucose use resulting from cellular insensitivity to the normal action of insulin-->hyperglycemia and hyperinsulinemia
insulin depends on the kidneys for excretion, therefore, diabetics with CKD may need ______ insulin than before the onset of CKD
hyperinsulinemia stimulates hepatic production of
therefore, almost all pts with uremia develop dyslipidemia r/t decreased levels of lipoprotein lipase that is important in the breakdwn of lipoproteins. This means that many pts with CKD die of Cardiovascular disease.
what serum potassium level is fatal?
If you are retaining sodium in renal failure, then why do you have hyponatremia and not hypernatremia?
bc of the excessive amount of fluid--dilutional hyponatremia
what is the sodium restriction for CKD
absence of reflexes, decreased mental status, cardiac dysrhythmias, hypotension, and respiratory failure
hypermagnesemia in CKD
which type of anemia is associated with CKD?
normocytic, normochromic anemia. due to decreased production of erythropoietin by the kidneys.
nutritional def's, decreased RBC lifespan, increased hemolysis of RBC, frequent blood samplings, and bleeding from GI tract add to anemia
What about PTH and CKD?
parathyroid hormone is increased in CKD to compensate for decreased Ca++ and HD. PTH inhibits erythropoeisis, shorten survival of RBCs and cause bone marrow fibrosis
PTH stimulated bone demineralization (increased fractures) to release Ca++ from bones, but this releases phosphate too and phosphate decreases vit D activation by kidneys too.
What about iron in CKd?
folic acid, essential for RBC maturation, is dialyzable bc it is water soluble. Give folic acid 1mg/day
Why is there so much bleeding with uremia and CKD?
defect in platelet fxn-impaired platelet aggregation and impaired release of platelet factor III. Alterations in the coagulation system with increased concentrations of factor VIII and fibrinogen=bleeding
Why do pts with CKD get so many infections?
decreased leukocyte production (enlarged spleen) as well as hyperglycemia and use of catheters, needle insertions, etc
which would you expect to see in a HD pt? left or right sided HF?
Left sided, esp left ventricular hypertrophy due to so much fluid to overcome to pump out
friction rub, chest pain, low grade fever
why is serum calcium low in CKD?
as kidney fxn deteriorates, less vit D is converted to its active form, resulting in decreased serum levels. To absorb Ca++ from GI tract, activated vit D is needed. Thus decreased active vit D levels result in less Ca++ absorption from GI and therefore decreased serum Ca++
CKD mineral and bone disorder
adds to morbity and mortaltiy risks bc the phosphate and calcium released from bone by PTH bind together and deposit on walls of vasculature (this may occur in the heart and disrupt conduction)
what happens to the skin with CKD?
pruritis, itchy, dry, uremic frost
first indication of kidney damage
proteinuria-do dipstick eval of protein in urine or evaluation for microalbuminuria (not detected on routine urinalysis)
a ratio greater than 300 mg albumin per 1 g Cr
meds for CKD
calcium supplements and/or phosphate binders, iron
ACEIs or ARBs
statins for hyperlipidemia
when do you take phosphate binders?
when do you take calcium supplements?
on an empty stomach, but NOT with iron
when do you take iron?
dyspnea, tachypnea, and SOB
indicators of fluid excess
what is dialysis for
to correct fluid and electrolyte imbalances in pts with kidney failure
Which dialysis is preferrable for a diabetic CKD patient?
inflow (10 mins) , dwell (20-30 mins), drain (15-30mins)
why implant an AVG over AVF?
history of IV drug abuse, obesity, or PVD
when can you use an AVF?
4-6 weeks, but recommendation is 3 months
when can you use AVG?
what is steel syyndrome
development of distal ischemia r/t HD access
Where do you access for HD while waiting for AVF or AVG?
Internal jugular or femoral percutaneous cannulation
1-3 weeks if in jugular, only 1 week in femoral
how do you treat hypotension during dialysis?
decrease volume of fluid being removed and infuse NS
What two nutritional supplements do you commonly give pts with CKD?
calcium and iron (iron causes constipation)
What happens to Hgb when dehydrated?
Hgb increases when dehydrated
dizziness, weakness, cardiac irregularities, muscle cramps, diarrhea, nausea
hyperkalemia (during oliguric phase)-->avoid giving pts with renal insufficiency potassium sparing diuretics, potassium supplements, or salt substitutes
use LASIX instead
fatigue, anorexia, dyspnea, nocturia, 1+pedal edema, basilar crackles in both lungs, clear pale urine, yellow gray pallor (due to anemia or uremia) bruising and uremic frost
What is protein restricted in renal patients
to reduce the accumulation of waste products associated with protein metabolism, which causes the manifestations of uremia. allowed proteins should be of high biologic value, such as eggs. Fluid allowances should be 500-600mL more than the previous days 24 hr urine output.
What is a big risk for HD patients?
could get hepatitis
What about weight gain and dialysis patients?
weight gain between dialysis should not exceed 1.5 kg
Nursing considerations for patient post op for kidney transplant?
Priority nursing diagnosis is risk for infection bc immunosuppressant meds are prescribed to decrease organ rejection, but also increase risk for infection. NO FLOWERS in patient room and frequent hand washing performed by all visitors
kidney pan, oliguria or anuria, HTN, lethargy, fever and fluid retention, increased BUN/Cr, increased Potassium
symptoms indicative of organ rejection
occurs within the first 48 hours of transplantation and requires immediate removal of transplanted kidney
occurs up to 2 years after surgery, most commonly within first 2 weeks. It can often be managed effectively with increased doses od immunosuppressice meds
a gradual process, occurring or a period of months to years. Conservative mgmt, including a careful balance of fluid and protein intake helps control the rejection, but the eventual outcome is the need for dialysis
raises BP as a result of angiotensin (local vasoconstriction) and aldosterone (volume expansion) secretion
renin produced in kidney
regulate intrarenal blood flow by vasodilation or vasoconstriction
prostaglandins produced by kidney
increase blood flow (vasodilation) and vascular permeabilty
bradykinins produced in kidney
stimulates bone marrow to make RBC
erythropoietin make in kidney
promotes absorption of calcium in the GI tract
Activated Vit D by kidney
makes DCT and CD permeable to water to maximaize reabsorption and produce a concentrated urine
ADH aka vasopressin (influenced by renal fxn) comes from posterior pituitary
promotes sodium reabsorption and potassium secretion in DCT and CD; water and chloride follow sodium
aldosterone (influenced by renal fxn) comes from adrenal cortex
cause tubular secretion of sodium
natriuretic hormones (influenced by renal fxn but made in cardiac atria and brain)
what is a nursing consideration for phosphate binders such as amphogel, alternaGEL?
aluminum toxicity may cause bone disease and dementia
nausea, vomiting, anorexia, visual disturbances, restlessness, HA, cardiac dysrhythmias, bradycardia
nursing considerations for Epogen
monitor Hct weekly-no more than 4 point increase in less than 2 weeks
explain that pelvic and limb pain should dissipate in 12 hours
dont shake vial as that mat inactivate glycoprotein
abnormal calcium metabolism causes bone pathology
What diagnostic tests allows you to determine kidney function?
IVP Intravenous Puelogram
Which diagnostic test allows you to determine bladder function?
Which diagnostic test allows you to determine bladder or urethral abnormalities?
What is a key patient teaching regarding resolution of aUTI?
Tell the client to be diligent about taking antibiotics around the clock and to not skip doses in order to keep blood level of antibiotic constant for optimal effectiveness.